The immunologic nature of tumor-associated transplantation antigens (TATA) of MM102 mammary tumor that originated spontaneously in C3H/He (H-2k) mice was analyzed. The TATA of MM102 tumor have been demonstrated in our laboratory to induce preferential generation of helper T cell activity without any significant killer T cell generation. The helper T cells that were generated by the immunization of syngeneic C3H/He mice with MM102 tumor and specifically reactive to the TATA of MM102 tumor were also reactive with the cellsurface antigens present on the normal or malignant lymphoid cells of allogeneic C57BL/6 (B6) and C57BL/10 (B10) mice. The reactivities of such TATA-reactive helper T cells were eventually the same irrespective of whether those lymphoid cells are derived from B10 (H-2b) mice or B10.BR (H-2k), the congenic strain of the same B10 background. Furthermore, in addition to the fact that the immunization of C3H/He mice with those lymphoid cells could induce the resistance against the challenge with viable MM102 cells, C3H/He mice that had been neonatally rendered tolerant to B10.BR could not develop the immune resistance against MM102 tumor.

These results clearly indicate that TATA of MM102 tumor are closely similar or identical to the non-H-2 antigens of allogeneic B10 mice on the level of helper T cell recognition, and that those non-H-2 alloantigens are capable of acting as the adequate transplantation antigens required for the effective induction of immune resistance against MM102 tumor.

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This work was supported by a Grant-in Aid for Cancer Research from the Ministry of Education, Science and Culture, Japan.

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